Cardiac Arrhythmias

Posted by e-Medical PPT
SA Node and AV node cells are slow conductors activated by calcium, thus blocked by calcium channel blockers such as verapamil.Atrium, Bundle of His, and ventricle cells are fast conducting and activated by sodium, thus blocked by sodium channel blockers (class 1 anti-arrhythmics) such as quinidine, lidocaine and propafenone.
Four Mechanisms of Arrhythmia
Reentry (most common)
Triggered activity

Reentry Requires
2 distinct pathways that come together at beginning and end to form a loop. 
A unidirectional block in one of those pathways. 
Slow conduction in the unblocked pathway.  

Reentry Mechanism
An arrhythmia is triggered by a premature beat
The fast conducting pathway is blocked because of its long refractory period so the beat can only go down the slow conducting pathway
The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway
On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement.  This creates the re-entry circuit

Heart cells other than those of the SA node depolarize faster than SA node cells, and take control as the cardiac pacemaker. 
Parasystole is a benign type of automaticity problem that affects only a small region of atrial or ventricular cells. 

Triggered activity
 is like a domino effect where the arrhythmia is due to the preceding beat. 
 Delayed after-depolarizations arise during the resting phase of the last beat and may be the cause of digitalis-induced arrhythmias. 
 Early after-depolarizations arise during the plateau phase or the repolarization phase of the last beat and may be the cause of torsades de pointes (ex. Quinidine induced)

Share Medical Presentations